County Health Leadership Practices and Readiness for Noncommunicable Disease Services in Kenya.

Background: Premature mortality from noncommunicable diseases (NCDs) is a contemporary development challenge. Low-income and lower-middle-income countries are disproportionately affected, with the poorest in society considered the most vulnerable. A paucity of literature exists on how leadership practices at the implementation level relate to ensuring readiness for NCD services. Objective: This study investigated any relationship between leadership practices and readiness for NCD services. Methods: This correlational study investigated any relationship between leadership practices at the county level and readiness for NCD services in Kenya using secondary data from a 2013 Service Availability and Readiness Assessment survey. Correlation and multiple linear regression tests were used to determine the strength and direction of any relationship between leadership practices (annual work planning, therapeutic committees, and supportive supervision), and NCD readiness (county readiness score). Findings: The findings indicated a statistically significant relationship between therapeutic committee (p = .002) and supportive supervision practices (p = .023) and NCD readiness. Leadership practices also had a statistically significant predictive relationship with NCD readiness (p = .009). Conclusion: Health leaders should ensure that leadership practices that have a predictive relationship with NCD readiness, such as therapeutic committee activities and supportive supervision visits, are implemented appropriately. Further, county health leaders should pay particular attention to the implementation of these leadership practices at nonpublic and Tiers 2, 3, and 4 health facilities that had lower NCD readiness scores.

Complex Structural PPT1 Variant Associated with Non-syndromic Canine Retinal Degeneration.

Rod and cone photoreceptors are specialized retinal neurons that have a fundamental role in visual perception, capturing light and transducing it into a neuronal signal. Aberrant functioning of rod and/or cone photoreceptors can ultimately lead to progressive degeneration and eventually blindness. In man, many rod and rod-cone degenerative diseases are classified as forms of retinitis pigmentosa (RP). Dogs also have a comparable disease grouping termed progressive retinal atrophy (PRA). These diseases are generally due to single gene defects and follow Mendelian inheritance.We collected 51 DNA samples from Miniature Schnauzers affected by PRA (average age of diagnosis ∼3.9 ±1 years), as well as from 56 clinically normal controls of the same breed (average age ∼6.6 ±2.8 years). Pedigree analysis suggested monogenic autosomal recessive inheritance of PRA. GWAS and homozygosity mapping defined a critical interval in the first 4,796,806 bp of CFA15. Whole genome sequencing of two affected cases, a carrier and a control identified two candidate variants within the critical interval. One was an intronic SNV in HIVEP3, and the other was a complex structural variant consisting of the duplication of exon 5 of the PPT1 gene along with a conversion and insertion (named PPT1dci ). PPT1dci was confirmed homozygous in a cohort of 22 cases, and 12 more cases were homozygous for the CFA15 haplotype. Additionally, the variant was found homozygous in 6 non-affected dogs of age higher than the average age of onset. The HIVEP3 variant was found heterozygous (n = 4) and homozygous wild-type (n = 1) in cases either homozygous for PPT1dci or for the mapped CFA15 haplotype. We detected the wildtype and three aberrant PPT1 transcripts in isolated white blood cell mRNA extracted from a PRA case homozygous for PPT1dci , and the aberrant transcripts involved inclusion of the duplicated exon 5 and novel exons following the activation of cryptic splice sites. No neurological signs were detected among the dogs homozygous for the PPT1dci variant. Therefore, we propose PPT1dci as causative for a non-syndromic form of PRA (PRA PPT1 ) that shows incomplete penetrance in Miniature Schnauzers, potentially related to the presence of the wild-type transcript. To our knowledge, this is the first case of isolated retinal degeneration associated with a PPT1 variant.

Lafora disease as a cause of visually exacerbated myoclonic attacks in a dog.

An 8-year-old, castrated male, miniature wire-haired dachshund was presented with a 4-month history of intermittent facial twitching (myoclonus). The myoclonic episodes progressed over a 16-month period. Generalized seizure activity was infrequent. Clinical examination revealed visually stimulated myoclonus. Response to therapy with antiepileptic drugs was equivocal. Genetic testing identified the dog as being affected by Lafora disease.

Postenucleation orbital sialocele in a dog associated with prior parotid duct transposition.

An orbital sialocele developed in a dog following enucleation for protracted glaucoma. This eye had historically been treated for keratoconjunctivitis sicca by parotid duct transposition approximately 5 years previously, and the duct was ligated distally at the time of enucleation. One month following enucleation, the dog presented with a fluctuant conical-shaped swelling ventrolateral to the orbital socket. Surgical exploration revealed a dilated, fibrotic distal portion of the previously transposed parotid duct, and saliva, within the enucleated orbit. The distal portion of the duct and saliva-containing tissues from within the orbit were excised. The remaining proximal normal portion of the parotid duct was re-routed into the oral cavity. Clinicopathologic and histologic examination of the excised orbital contents and dilated portion of duct revealed a sterile sample of saliva and moderate chronic periductal fibrosis. At a 6-month re-evaluation there was no evidence of recurrence of the sialocele, and the parotid duct was functional.

Classification of feline intraocular neoplasms based on morphology, histochemical staining, and immunohistochemical labeling.

The objectives of this study were to evaluate morphologic, histochemical, and immunohistochemical characteristics of well-differentiated and anaplastic intraocular neoplasms of cats, and to develop a diagnostic algorithm for, and investigate the association of ruptured lenses with these neoplasms. Seventy-five feline globes with intraocular neoplasms were stained with hematoxylin and eosin and examined by light microscopy. Morphologic diagnoses included 33 intraocular sarcomas, 17 diffuse iris melanomas, 15 lymphosarcomas, three ciliary adenomas, one metastatic carcinoma, and six undifferentiated intraocular neoplasms. Sections of these globes were then stained with periodic acid Schiff (PAS), and immunohistochemical (IHC) labels for various cellular markers. Histochemical staining and IHC labeling confirmed cellular differentiation in 73/75 neoplasms but was discordant with morphologic diagnoses in 8/75. These included four neoplasms morphologically diagnosed as lymphosarcomas but which expressed differentiation antigens consistent with melanoma (n = 3) or ciliary adenocarcinoma (n = 1), and four tumors morphologically diagnosed as intraocular sarcomas that expressed differentiation antigens for melanoma (n = 2), metastatic carcinoma (n = 1), or remained undifferentiated (n = 1). Immunohistochemical labeling suggested a diagnosis in 5/6 morphologically undifferentiated neoplasms including one intraocular sarcoma, two diffuse iridal melanomas, and two ciliary adenocarcinomas. Based upon morphologic, histochemical, and IHC characterization, ruptured lens capsules were detected in 28/30 intraocular sarcomas, 3/24 diffuse iris melanomas and 1/11 lymphosarcomas, but not in ciliary epithelial neoplasms, metastatic carcinomas, or undifferentiated intraocular neoplasms. An algorithm is provided that facilitates stain and IHC label selection for differentiating anaplastic intraocular feline neoplasms.

Brainstem auditory evoked responses and ophthalmic findings in llamas and alpacas in Eastern Canada.

Seventeen llamas and 23 alpacas of various coat and iris colors were evaluated for: (1) deafness by using brainstem auditory evoked response testing; and (2) for ocular abnormalities via complete ophthalmic examination. No animals were deaf. The most common ocular abnormalities noted were iris-to-iris persistent pupillary membranes and incipient cataracts.

Intracranial meningioma causing internal ophthalmoparesis in a dog.

A 10-year-old, spayed female, Irish water spaniel was presented with a 2-week history of anisocoria characterized by mydriasis of the right eye compared to the left eye in ambient light. Ophthalmic and neurological examinations, combined with pharmacological testing, identified a disease process affecting the right parasympathetic nucleus of cranial nerve 3 (CN III) and/or the parasympathetic component of CN III. Magnetic resonance imaging (MRI) identified a mass involving the right midbrain and extending caudally to the rostral border of the medulla oblongata. The dog became comatose within 12 h following MRI and was euthanized. Histopathology identified the intracranial mass as a meningioma.

Ultrastructural findings in feline corneal sequestra.

OBJECTIVES: (1) To describe the ultrastructural features of corneal sequestra in cats; and (2) to enhance our understanding regarding the pathogenesis of feline corneal sequestration. METHODS: Nine corneal sequestra were harvested via keratectomy from globes of nine cats. The sequestra were routinely fixed then postfixed for high resolution light and transmission electron microscopy (HR-LM and TEM, respectively). The tissues were embedded in Epon/Araldite. Sections of 0.5-microm thickness were cut and stained with 1% toluidine blue in 1% sodium tetraborate solution for HR-LM. Ultrathin sections were collected on copper grids and stained with uranyl acetate and Sato's lead stain for TEM. Ultrathin sections were examined and the images were captured on an Advantage HR CCD camera using a Hitachi 7500 electron microscope operated at 80 kV. Two healthy corneas from two cats were harvested immediately following euthanasia. These corneal tissues (control samples) were processed in the same manner as the corneal sequestra for HR-LM and TEM. A portion of each sequestrum was also submitted for polymerase chain reaction (PCR) testing for infectious agents including feline herpesvirus-1 (FHV-1), Toxoplasma gondii, Chlamydophila felis and Mycoplasma spp. RESULTS: Ultrastructure of healthy corneal tissues revealed basal corneal epithelial cells aligned adjacent to a thin acellular layer similar to Bowman's layer with underlying tightly packed, regularly arranged, collagen fibrils oriented in different planes. Keratocytes were elongated and had long and irregularly shaped nuclei, and cytoplasm contained rough endoplasmic reticulum and abundant membrane-bound vesicles. In contrast, corneal sequestra contained varying amounts of an amorphous, electron-dense substance, continuous with intact basal epithelial basement membranes peripherally, and overlying corneal ulceration and loosely packed collagen fibrils. Remnants of necrotic keratocytes were seen in spaces between disarranged collagen layers. In all samples, occasional keratocytes exhibited morphology indicative of apoptosis including clumping and margination of chromatin, and shrunken cytoplasm. Varying degrees of inflammation were noted on HR-LM and TEM of affected corneas including peri- and intralesional neutrophils, lymphocytes, plasma cells, and macrophages. Corneal sequestra were FHV-1-positive (n = 3), FHV-1- and T. gondii-positive (n = 1), T. gondii-positive (n = 3), or negative for DNA of these infectious agents (n = 2) using PCR. All corneal sequestra were negative for DNA of Chlamydophila felis and Mycoplasma spp. using PCR. CONCLUSIONS: Apoptosis may play a role in the pathogenesis of feline corneal sequestration independent of the presence of DNA of these infectious organisms. Prospective clinical studies are warranted to further understand the significance of T. gondii in relation to feline corneal sequestration.

Schirmer tear test values and tear film break-up times in cats with conjunctivitis.

OBJECTIVES: (1) To document tear film break-up time (TFBUT) in a group of cats with conjunctivitis; (2) to determine if TFBUTs from cats with conjunctivitis vary significantly from previously established normal values for TFBUT in young cats without ocular disease; (3) to determine if a correlation exists between Schirmer tear test (STT) values and TFBUTs in cats with conjunctivitis; (4) to determine if the TFBUTs in cats with conjunctivitis are influenced by the detection of DNA from feline herpes virus-type 1 (FHV-1), Chlamydophila felis, Mycoplasma spp., and feline calicivirus. ANIMALS STUDIED: Fourteen cats between the ages of 0.8 years to 12 years with active, untreated conjunctivitis and without active keratitis or other ocular or systemic abnormalities were included in this study. Procedures Complete ophthalmic examinations, including TFBUT, were performed on all cats. Polymerase chain reaction (PCR) screening for FHV-1, Chlamydophila felis, Mycoplasma spp., and feline calicivirus was performed on conjunctival swabs from affected eyes and blood samples from all cats. RESULTS: Mean TFBUT for cats in this study was 8.9 (+/- 4.8) s in the right eye (OD) and 8.1 (+/- 4.6) s in the left eye (OS). No correlation existed between mean TFBUTs and mean STT values OD or OS. Conjunctival swabs from seven cats (n = 9 eyes) tested positive via PCR for one of the above infectious agents. Blood samples from nine cats tested positive for FHV-1. Mean TFBUTs for cats from which the DNA from FHV-1 was isolated from the blood were significantly lower than mean TFBUTs for cats from which no such DNA was isolated from the blood. CONCLUSIONS: In this study, the mean TFBUT in cats with conjunctivitis was significantly lower than previously established values for clinically healthy cats. This supports the theory that qualitative tear film deficiency, and thus tear film instability, may play a role in the pathogenesis of feline conjunctivitis. Qualitative tear film deficiency may predispose to the development of conjunctivitis or may occur secondarily to this condition.

Keratoconjunctival effects of diabetes mellitus in dogs.

OBJECTIVES: To compare Schirmer tear test (STT) values, corneal sensitivity, tear film break up times (TFBUTs), and tear glucose concentrations in relation to conjunctival microflora, and conjunctival cytologic and histologic findings among diabetic cataractous, nondiabetic cataractous, and nondiabetic noncataractous dogs. Procedures Fifteen dogs in each category underwent neuro-ophthalmic examination; aerobic, anaerobic and fungal conjunctival cultures; assessment of corneal touch threshold (CTT), STT, tear glucose, TFBUT; and conjunctival cytology and histology (in certain cases only). Degree of cataract and uveitis were critically graded. Glycemic control was estimated using serum fructosamine and glycosylated hemoglobin. RESULTS: STT values were significantly lower in diabetic cataractous than nondiabetic noncataractous dogs. CTT of diabetic cataractous dogs was significantly lower than that of nondiabetic noncataractous dogs. Mean TFBUTs were significantly less in diabetic cataractous dogs than nondiabetic cataractous and nondiabetic noncataractous dogs. Tear glucose concentrations were significantly higher in diabetic cataractous dogs than nondiabetic cataractous and nondiabetic noncataractous dogs. Conjunctival microbial isolates did not differ among groups. There were no significant differences in degree of cataract or uveitis between diabetic cataractous and nondiabetic cataractous groups. There was mild submucosal inflammatory infiltrate in conjunctival specimens from diabetic dogs. Conjunctival epithelial dysplasia and/or squamous metaplasia was/were detected in conjunctival biopsies of 5/7 diabetic dogs. Reductions in conjunctival goblet cell (GC) densities were noted in 4/7 diabetic dogs; there were no significant differences in mean GC densities among the three groups. CONCLUSIONS: Diabetic cataractous dogs have significantly altered keratoconjunctival characteristics compared to nondiabetic cataractous and nondiabetic noncataractous dogs.

Tear film breakup times in young healthy cats before and after anesthesia.

The objectives of this study were: (i) to determine tear film breakup times (BUTs) in young healthy cats; (ii) to determine tear film BUTs in feline eyes within 8-20 h following general anesthesia; (iii) to determine if tear film BUTs vary significantly preoperatively when compared with values obtained 8-20 h postoperatively; (iv) to determine if Schirmer tear test (STT) values correlate with tear film BUTs in young healthy cats; and (v) to determine if the isolation of particular etiologic agents from conjunctival swabs of healthy cats affects tear film BUTs. We studied eighteen healthy Domestic Short-haired (n=14) and Domestic Long-haired (n=4) cats, with normal ocular examinations, ranging in age from 0.5 to 3 years. Complete ophthalmic examinations, including tear film BUTs, were performed on all cats. Conjunctival swabs from each eye of all cats and blood samples from all cats were collected and submitted for polymerase chain reaction screening for feline herpes virus, Chlamydophila felis, Mycoplasma spp., and calicivirus. In 10 of 18 cats, STT values and tear film BUTs were measured before general anesthesia was administered and again within 8-20 h following the end of anesthesia. Mean preanesthesia tear film BUTs for all 18 cats were 17.4+/-4.6 s OD and 16.0+/-4.5 s OS. Mean postanesthesia tear film BUT results were 12.5+/-4.3 and 13.1+/-4.0 s OD and OS, respectively. Postanesthesia tear film BUTs were significantly more rapid than those measured before anesthesia (OD only). There was also a positive correlation, both before and after anesthesia, between STT values in both eyes (OU) and tear film BUTs OU. The isolation or lack of isolation of conjunctival microorganisms using PCR did not significantly affect tear film BUTs. Mean tear film BUT in young healthy domestic cats is 16.7+/-4.5 s. Tear BUT is positively correlated with STT values. Although mean tear film BUTs OD at 8-20 h following anesthesia were more rapid than preanesthesia values, this difference did not appear clinically relevant.